Background: Esmolol is rapid hydrolyzed by plasma esterase but may inhibit plasma cholinesterase activity based on its structure. This study was designed to evaluate the interactions between esmolol and succinylcholine or mivacurium which are metabolized by plasma cholinesterase and to determine the inhibitory effect of esmolol on human plasma cholinesterase. Methods: Neuromuscular effects of succinylcholine (1.0 mg/kg) and mivacurium (0.15 mg/kg) with or without esmolol (0.5 mg/kg or 1.0 mg/kg) were compared in 57 adult patients (ASA class I) during O2-N2O-isoflurane anesthesia. Neuromuscular block was monitored by recording the compound electromyogram of the hypothenar muscle resulting from supramaximal train of four stimuli applied to the ulnar nerve. Also plasma cholinesterase activity was measured before and 5, 10 minutes after injection of esmolol. Results: Time from injection to onset of over 95% block, clinical duration from injection to 25% recovery of control twitch, and recovery index defined as from 25% to 75% twitch recovery of succinylcholine or mivacurium were not altered by pretreatment of esmolol. Plasma cholinesterase activity was not decreased after injection of esmolol 0.5 mg/kg, but decreased by 5% after injection of 1.0 mg/kg (p<0.05). Conclusions: It is unlikely that neuromuscular blocking effects of succinylcholine and mivacurium are prolonged by administration of clinical doses of esmolol (0.5~1.0 mg/kg) due to inhibition of plasma cholinesterase activity in human.
Adult ; Anesthesia ; Cholinesterases ; Humans ; Neuromuscular Agents ; Neuromuscular Blockade ; Plasma ; Succinylcholine* ; Ulnar Nerve

No abstract available.
Electrocardiography, Ambulatory*

OBJECTIVE: This study was conducted to elucidate neuroprotective effect of carnosine in early stage of stroke. METHODS: Early stage of rodent stroke model and neuroblastoma chemical hypoxia model was established by middle cerebral artery occlusion and antimycin A. Neuroprotective effect of carnosine was investigated with 100, 250, and 500 mg of carnosine treatment. And antioxidant expression was analyzed by enzyme linked immunosorbent assay (ELISA) and western blot in brain and blood. RESULTS: Intraperitoneal injection of 500 mg carnosine induced significant decrease of infarct volume and expansion of penumbra (p<0.05). The expression of superoxide dismutase (SOD) showed significant increase than in saline group in blood and brain (p<0.05). In the analysis of chemical hypoxia, carnosine induced increase of neuronal cell viability and decrease of reactive oxygen species (ROS) production. CONCLUSION: Carnosine has neuroprotective property which was related to antioxidant capacity in early stage of stroke. And, the oxidative stress should be considered one of major factor in early ischemic stroke.
Anoxia ; Antimycin A ; Blotting, Western ; Brain ; Carnosine* ; Cell Survival ; Enzyme-Linked Immunosorbent Assay ; Infarction, Middle Cerebral Artery ; Injections, Intraperitoneal ; Ischemia* ; Neuroblastoma ; Neurons ; Neuroprotective Agents* ; Oxidative Stress ; Reactive Oxygen Species ; Rodentia* ; Stroke ; Superoxide Dismutase

The purpose of the present study was to determine whether chronic high-fat diet (HF) induces insulin resistance independently of obesity. We randomly divided 40 rats into two groups and fed them either with a HF or with a high-carbohydrate diet (HC) for 8 weeks. Whole body glucose disappearance rate (Rd) was measured using a euglycemic hyperinsulinemic clamp. Firstly, we defined whether insulin resistance by HF was associated with obesity. Plasma glucose and triglyceride concentrations were significantly increased in HF. Rd was decreased (10.6+/-0.2 vs. 9.1+/-0.2 mg/kg/min in HC and HF, respectively) and the hepatic glucose output rate (HGO) was increased in HF (2.2+/-0.3 vs. 4.5+/-0.2 mg/kg/min in HC and HF, respectively). Rd was significantly correlated with %VF (p<0.01). These results implicate that visceral obesity is associated with insulin resistance induced by HF. In addition, to define whether dietary fat induces insulin resistance regardless of visceral obesity, we compared Rd and HGO between groups 1) after matching %VF in both groups and 2) using an ANCOVA to adjust for %VF. After matching %VF, Rd in HF was significantly decreased by 14% (p<0.001) and HGO was significantly increased by 110% (p<0.001). Furthermore, statistical analyses using an ANCOVA also showed Rd for HF was significantly decreased even after adjusting %VF. In conclusion, we suggest that dietary fat per se could induce insulin resistance in rats fed with chronic HF independently of obesity.
Adipose Tissue/*pathology ; Animal ; Dietary Carbohydrates/administration &age ; Dietary Fats/*administration &age ; Fatty Acids, Nonesterified/metabolism ; Female ; *Insulin Resistance ; Obesity/etiology ; Rats ; Rats, Sprague-Dawley ; Viscera

No abstract available.
Clone Cells* ; Cloning, Organism* ; DNA* ; Flagellin* ; Helicobacter pylori* ; Helicobacter* ; Sequence Analysis, DNA*

PURPOSE: Polypoid lesions of the gall bladder (PLG) have a variety of pathologies. Problems exist in the selection of patients for operation and in the operative approach used. We studied the accuracy of the preoperative radiologic diagnosis and suspected risk factors. METHODS: 121 polypoid lesions of gallbladder were sugically treated during 10 years. Preoperative radiologic diagnosis, age, gender, related symptoms, concurrent gallstone, size, shape, number and histologic diagnosis of the ployps were retrospectively reviewed. RESULTS: The average size of malignancy was 23.0 mm, and that of benign tumors was 7.1 mm (P=0.000). The mean age of patients with a malignancy was significant higher than that of those with benign tumor (P=0.000). The preoperative sensitivity of computed tomography for a malignancy was 67.7%. The patients with malignancy more frequently had related symptoms. CONCLUSION: A CT must be considered, for patients with risk factors, even if the ultrasonographic diagnosis was benign. An Age greater than 60 years, a tumor size greater than 10 mm, a solitary polyp, sessile shape, and related symptoms are predictive factors of a malignancy.
Diagnosis ; Gallbladder* ; Gallstones ; Humans ; Pathology ; Polyps ; Retrospective Studies ; Risk Factors ; Urinary Bladder

No abstract available.
Factor VII Deficiency* ; Factor VII*

We examined the effect of leptin on the insulin resistance in skeletal muscles by measuring the glucose transport. Male Wistar rats were fed with chow or high-fat diets for 30 days. Three days before sacrifice, high-fat fed rats were subcutaneously injected with leptin (1 mg/kg body weight) for 3 days. The glucose transports in the epitrochlearis and soleus muscle were not different among the experimental groups under basal state, however these were decreased significantly in the high fat-diet rats under insulin-stimulation (P< 0.01). Leptin treatment recovered the decreased glucose transport in the epitrochlearis (P< 0.05) and soleus (p=0.08). Triglyceride concentration in the soleus muscle was increased significantly in the high fat-fed rats, compared to chow diet rats (P< 0.01), and it was decreased significantly by leptin treatment (P< 0.01). The glucose transport was measured under basal and 60microU/ml of insulin with or without 50 ng/ml of leptin. Leptin had no direct stimulatory effect on glucose transport under both basal and insulin-stimulated conditions in vitro. These results demonstrate that leptin injection to high fat diet fed rats recovered impaired insulin responsiveness of the skeletal muscles and muscle triglyceride concentration. However, there was no direct stimulatory effect of leptin on insulin sensitivity of the skeletal muscle in vitro.
Animals ; Diet ; Diet, High-Fat* ; Glucose ; Humans ; Insulin Resistance* ; Insulin* ; Leptin* ; Male ; Muscle, Skeletal* ; Rats* ; Rats, Wistar ; Triglycerides

Purpose: To study the risk factors for steroid-induced glaucoma patients requiring glaucoma surgery, despite being fully treated with medications and laser trabeculoplasty. Methods: The charts of 50 eyes diagnosed with steroid-induced glaucoma from January 2012 to December 2015 were reviewed retrospectively. 28 eyes required surgery and 22 eyes were successfully treated with medications and laser trabeculoplasty. The demographic information as well as ocular parameters, presence of ocular/systemic comorbidities, and past history of steroid use were evaluated to determine the risk factors associated with the need for glaucoma surgery. Results: For the 7 factors that were statistically significant by univariate regression analysis, multivariate regression analysis showed that the average retinal nerve fiber layer thickness and duration of steroid use were not statistically significant (p = 0.876 and p = 0.068, respectively), whereas age and initial intraocular pressure were only statistically significant in some of the analysis models (p = 0.040-0.278, p = 0.016-0.201, respectively). Myopia, vertical cup-to-disc ratio, and systemic comorbidities had statistically significant correlations (p = 0.019, p = 0.011-0.03, p = 0.022, respectively) with surgical decision by multivariate regression analysis. Conclusions The risk factors for requiring glaucoma surgery in steroid-induced glaucoma patients were young age, myopia, initial optic nerve damage, systemic disease (systemic lupus erythematosus, rheumatoid arthritis, and atopy), and duration of steroid use. These results may be helpful in predicting the prognosis of patients with steroid-induced glaucoma and in screening for patients who require a more aggressive treatment at the time of disease presentation.

We investigated the change in activity of the sympathetic nervous system (SNS) in high-sucrose diet (HSD)-induced obese rats compared with controls. Power spectral analyses of R-R interval variability were performed to obtain the low frequency (LF, 0.04-0.699 Hz) and high frequency (HF, 0.7-3.0 Hz) powers. The percents of fat mass to body weight (%F/BW) and fat to muscle ratios (F/M) were significantly increased in HSD-fed rats. Plasma glucose, leptin, and triglyceride concentrations in rats fed with HSD were significantly increased. LF in normalized units (LFn), which represents both sympathetic and parasympathetic activities, was significantly increased whereas HF in normalized unit (HFn), which represents parasympathetic activity, was significantly decreased in HSD-fed rats. LF/HF, which represents sympathetic activity, was significantly increased in HSD-fed rats and was correlated with leptin (r=0.549, p<0.023), %F/BW (r=0.513, p<0.035), F/M (r=0.536, p<0.038), and triglyceride (r=0.497, p<0.042). When adjusted for leptin concentrations, however, LF/HF of HSD-fed rats was significantly decreased. In conclusion, HSD-induced obese rats showed increased LF/HF, which was significantly decreased by adjustment for leptin concentrations. We suggest that stimulating effect of leptin on SNS is reduced, which might play a role in induction of obesity by HSD.
Animal ; Body Weight ; Dietary Carbohydrates/administration & dosage ; Disease Models, Animal ; Fats/metabolism ; Male ; Muscles ; Obesity/physiopathology* ; Obesity/metabolism ; Obesity/etiology ; Rats ; Rats, Wistar ; Spectrum Analysis, Mass/methods ; Sympathetic Nervous System/physiopathology*